DYNAMICS OF PULMONARY CIRCULATION 



1719 



table 3. Representative Oxygen Tensions oj Precapillary 

 and Postcapillary Pulmonary I 'essels During 

 I 'at urns Experimental Circumstant es 



Rest; ambient air 

 Moderate exercise; ambient air 

 Bilateral hypoxia; 12% 2 

 Unilateral hypoxia; 5% O: 



* Pulmonary venous P,,„ on the opposite side, i.e., the 

 hyperoxic side, exceeds 100 mm Hg. 



tion (132), and left atrial pressure (125, 303) — 

 undergo too little change to affect the level of pulmo- 

 nary arterial pressure, the increase in the blood pres- 

 sure gradient across the lungs is generally acknowl- 

 edged to involve an active increase in pulmonary 

 vascular resistance, i.e., vasoconstriction. 



In essence, the evidence for vasoconstriction during 

 acute hypoxia falls into three categories (132): /) the 

 disproportionate increase in the pressure gradient 

 across the lung with respect to the increment in 

 pulmonary blood flow (fig. 32) (132); .' ) the redistri- 

 bution of the pulmonary blood flow in favor of the 

 high-oxygen lung during unilateral hypoxia (209, 

 328, 408); and 2) the vasodilator effects of infused 

 acetylcholine during bilateral (153) and unilateral 

 (go) hypoxia. Despite this cumulative evidence, not 

 all are convinced that acute hypoxia elicits pulmo- 

 nary vasoconstriction (353). However, although the 

 evidence against pulmonary vasoconstriction is not 

 very substantial, it does serve to recall: a) that the 

 magnitude of the changes in pulmonary vascular 

 blood pressure is small; b) the possibility that subtle 

 extraneous influences, such as constriction of the 

 extravascular smooth muscle may mimic vasocon- 

 striction; and c) that the effects of acute hypoxia on 

 the pulmonary circulation are easily overwhelmed 

 by known mechanical influences, such as gravity 



('3 2 )- 



The particular vascular segment, or segments, in- 

 volved in the pulmonary vasoconstriction has been 

 sought in many ways. At the moment, the experi- 

 ments performed under exceedingly artificial condi- 

 tions favor postcapillary vasoconstriction. On the 

 other hand, experiments in intact animals with di- 

 nitrophenol (which selectively lowers precapillary 

 oxygen tension) have demonstrated precapillary vaso- 

 constriction (Bergofsky et al., unpublished observa- 

 tions). No evidence has yet been adduced to indicate 

 that pulmonary venous-left atrial junctions constrict 

 during hypoxia. The opinion of the author is that 



both the precapillary small vessels and the post- 

 capillary small vessels can constrict if exposed to a 

 sufficient degree of hypoxia (132). An idea of the 

 oxygen tensions which exist in the pre- and post- 

 capillary segments under various conditions is given 

 in table 3. 



The notion that the small pulmonary muscular 

 vessels, regardless of location, constrict when exposed 

 to a sufficiently intense hypoxic stimulus implies that 

 during ambient air breathing the hypoxic mixed 

 venous blood may set the tone (albeit slight) of the 

 pulmonary ''arterioles" and, thereby, the level of the 

 pulmonary arterial pressure; this tonic effect would 

 presumably be heightened during exercise (as mixed 

 venous blood becomes more unsaturated) unless the 

 arterioles were passively widened by mechanical 

 influences. The experiments involving hypoxia by 

 airway are also complicated. In these, the prospect 

 exists that the hypoxic mixture may affect the pre- 

 capillary as well as the postcapillary segments; none- 

 theless, the postcapillary segments would be more 

 drastically affected because mixed venous blood is 

 ordinarily low in oxygen tension. Finally, vasocon- 

 striction of either segment could account for some 

 rearrangement of the pulmonary blood flow in pa- 

 tients with maldistribution of air and blood even 

 though mechanical influences would be expected to 

 be prepotent. 



Several other aspects of the pressor response to 

 acute hypoxia warrant special emphasis: <;) the in- 

 crease in vascular resistance in the isolated perfused 

 lung — which is devoid of neurohumoral influences, of 

 a collateral circulation, and of extrapulmonary re- 

 flexes — indicates that hypoxia acts locally, i.e., either 

 by a direct chemo-effect on the vessel, or by way of an 

 intrapulmonary reflex, rather than by way of extra- 

 pulmonary controls (116, 305); b) the persistence of 

 the pressor response after ergotamine and atropine 

 favors a direct rather than a reflex action (116, 125); 

 c) severe hypoxia or anoxia, as commonly used in the 

 isolated lung or in artificial preparations, may not 

 represent the same biochemical stimulus to vascular 

 smooth muscle as tolerable levels of hypoxia in animal 

 or man (132); d) the pulmonary vasoconstriction 

 evoked by hypoxia has to be reconciled with the fact 

 that hypoxia dilates most intact vascular beds, con- 

 stricts isolated vessels, and dilates the placental 

 vessels (137); e) the biochemical mechanism by which 

 acute hypoxia causes smooth muscle to constrict has 

 not been elucidated (116);/) the catecholamines are 

 not involved in the pressor response to moderate 

 hypoxia (163); andjj) the vasoconstriction evoked by 



